Paracetamol (acetaminophen) produces analgesia and antipyresis without significant anti-inflammatory action. Its central mechanism and its dangerous metabolite are best described as:

• A Blockade of both COX and 5-lipoxygenase; toxic metabolite is leukotriene B4
• B Peripheral COX-1 inhibition in platelets; toxic metabolite is salicylic acid
• C Inhibition of phospholipase A2 centrally; toxic metabolite is glutathione disulfide
• D Central COX inhibition favoured in the peroxidase-poor CNS environment; toxic metabolite is N-acetyl-p-benzoquinone imine ✓

Explanation

Paracetamol weakly inhibits cyclooxygenase but acts preferentially in the brain, where low peroxide tone permits COX blockade, explaining antipyresis and analgesia with minimal peripheral anti-inflammatory effect. About 5 percent of the dose becomes N-acetyl-p-benzoquinone imine (NAPQI), which depletes hepatic glutathione and causes centrilobular necrosis; N-acetylcysteine replenishes glutathione. Platelet COX-1 inhibition is the domain of aspirin, ruling out option B.

Reference: Katzung Basic and Clinical Pharmacology, 16th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.